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瑞士乳杆菌和长双歧杆菌联合使用可降低心肌梗死后大鼠模型边缘系统的细胞凋亡倾向。

Lactobacillus helveticus and Bifidobacterium longum taken in combination reduce the apoptosis propensity in the limbic system after myocardial infarction in a rat model.

机构信息

Centre de Biomédicine, Hôpital du Sacre-Coeur de Montréal, 5400 Boulevard Gouin Ouest, Montréal, Que., Canada H4J 1C5.

出版信息

Br J Nutr. 2009 Nov;102(10):1420-5. doi: 10.1017/S0007114509990766. Epub 2009 Jun 29.

Abstract

Myocardial infarction (MI) stimulates the release of pro-inflammatory substances that induce apoptosis in the limbic system. Pro-inflammatory cytokines are considered as the root cause of apoptosis, although the mechanism is not fully explained and/or understood at this time. In addition, depression may induce gastrointestinal perturbations that maintain the elevated levels of pro-inflammatory cytokines. It has been shown that some specific probiotic formulations may reduce gastrointestinal problems induced by stress and the pro/anti-inflammatory cytokine ratio. Therefore, we hypothesised that probiotics, when given prophylactically, may diminish the apoptosis propensity in the limbic system following a MI. Male adult Sprague-Dawley rats were given probiotics (Lactobacillus helveticus and Bifidobacterium longum in combination) or placebo in their drinking-water for four consecutive weeks. A MI was then induced in the rats by occluding the left anterior coronary artery for 40 min. Rats were killed following a 72 h reperfusion period. Infarct size was not different in the two groups. Bax/Bcl-2 (pro-apoptotic/anti-apoptotic) ratio and caspase-3 (pro-apoptotic) activity were reduced in the amygdala (lateral and medial), as well as in the dentate gyrus in the probiotics group when compared with the placebo. Akt activity (anti-apoptotic) was increased in these same three regions. No significant difference was observed in Ca1 and Ca3 for the different markers measured. In conclusion, the probiotics L. helveticus and B. longum, given in combination as preventive therapy, reduced the predisposition of apoptosis found in different cerebral regions following a MI.

摘要

心肌梗死 (MI) 会刺激促炎物质的释放,这些物质会诱导边缘系统中的细胞凋亡。促炎细胞因子被认为是细胞凋亡的根本原因,但目前这一机制尚未得到充分解释和/或理解。此外,抑郁可能会引发胃肠道紊乱,从而维持促炎细胞因子的升高水平。已经表明,一些特定的益生菌配方可能会减少应激和促炎/抗炎细胞因子比值引起的胃肠道问题。因此,我们假设预防性给予益生菌可能会减少 MI 后边缘系统中的细胞凋亡倾向。雄性成年 Sprague-Dawley 大鼠连续四周在饮用水中给予益生菌(瑞士乳杆菌和长双歧杆菌的组合)或安慰剂。然后通过阻塞左前冠状动脉 40 分钟来诱导大鼠发生 MI。大鼠在 72 小时再灌注期后处死。两组的梗死面积无差异。与安慰剂组相比,益生菌组的杏仁核(外侧和内侧)和齿状回中的 Bax/Bcl-2(促凋亡/抗凋亡)比值和 caspase-3(促凋亡)活性降低。这些相同的三个区域中的 Akt 活性(抗凋亡)增加。在不同的标记物测量中,Ca1 和 Ca3 没有观察到显著差异。综上所述,作为预防性治疗给予的瑞士乳杆菌和长双歧杆菌益生菌组合减少了 MI 后不同脑区发现的细胞凋亡倾向。

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